We will investigate the chemical regulation of breathing in normal and obese volunteers awake and during slow-wave (SW) and rapid eye movement (REM) sleep. We will compare in each of these states: 1) hypoxic and hypercapnic sensitivity; 2) changes in the influence of hypoxia and hypercapnia on breathing; and 3) the distribution of respiratory output to pharyngeal and to skeletal muscles. Hypoxia and hypercapnia will be produced awake and asleep by steady state and rebreathing methods. Since airway resistance and chest wall mechanics change during sleep, respiratory efferent activity will be assessed from recordings of respiratory and pharyngeal muscle EMG, by measurements of ventilation, and by rib cage and abdominal movement. We will also examine the effects of loads on breathing and the effects of mechanical and chemical stimuli in causing arousal or switches in sleep stage. The data obtained will be used to amplify a mathematical model of the chemical control of breathing and to test the following hypotheses: 1) that depressed chemosensitivity in the awake state is associated with blunted responses to chemical stimulation that occur during sleep; 2) that central sleep apneas appear whenever peripheral chemoreceptor input dominates the activity of the central respiratory neurons and causes instability in control; 3) that obstructive apnea is promoted by unequal effects of chemical drive on the electrical activity of pharyngeal and inspiratory muscles; 4) that instability in control and resulting central sleep apnea increases the frequency of obstructive apnea, and the conversely obstructive apneas increase central apneas; 5) that irregularities in breathing are related to the effects of mechanical and chemical stimuli on sleep; and 6) that metabolic alkalosis and acidosis, which shift CO2 responses, will alter the occurrence of central and obstructive sleep apneas.